Apnoea of prematurity — short-answer question

Part A — Definition and pathophysiology (10 marks)

a) State the formal definition of apnoea of prematurity (2 marks)

Apnoea of prematurity is a cessation of breathing lasting 20 seconds or longer, or a shorter pause accompanied by bradycardia (a heart rate below 80 beats per minute), central cyanosis, or oxygen desaturation below roughly 80 to 85 percent. [2]

b) Describe the pathophysiology and the three types of apnoea (8 marks)

The pathophysiology rests on immaturity of the brainstem respiratory control centre, which fires with an irregular rhythm and weak central drive, so that the apnoeic threshold for carbon dioxide sits close to the resting level. [2]

Peripheral chemoreceptor responses to hypoxia are blunted and paradoxical, so hypoxia further depresses breathing rather than stimulating it. The highly compliant chest wall and low functional residual capacity favour airway closure and atelectasis, compounding desaturation. [2]

Three types are recognised. Central apnoea is absent effort with absent airflow from loss of neural drive. Obstructive apnoea preserves effort but loses airflow through upper-airway collapse during the dominant active sleep of prematurity. Mixed apnoea, a central pause followed by obstruction, is the most common form and explains why continuous positive airway pressure is often required alongside caffeine. [2]

Part B — Management (10 marks)

a) Outline the stepwise management and state the caffeine citrate doses (6 marks)

Confirm the event on the cardiorespiratory and SpO2 traces and exclude secondary causes. Begin with gentle tactile stimulation and repositioning. First-line pharmacotherapy is caffeine citrate at a loading dose of 20 mg/kg followed by maintenance of 5 to 10 mg/kg once daily. [1]

Add nasal continuous positive airway pressure or nasal intermittent positive-pressure ventilation for obstructive or mixed events. Reserve doxapram as a third-line rescue for refractory apnoea unresponsive to caffeine and non-invasive support. [1]

b) List the secondary causes you must exclude and explain the discharge and prognosis principles (4 marks)

Exclude sepsis (the most important, with a septic screen and blood culture), hypoglycaemia and electrolyte disturbance, anaemia, intraventricular haemorrhage, patent ductus arteriosus, and central depressant drugs. [2]

Most infants resolve by 36 weeks postmenstrual age, with resolution by 43 to 44 weeks expected in the extremely preterm. Apnoea of prematurity is not a risk factor for sudden infant death syndrome. Discharge requires an apnoea-free interval and stable feeding, typically around 34 to 36 weeks postmenstrual age; home monitoring is not routinely indicated. [3]